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"γc" cytokines are a family whose receptors share a "common-gamma-chain" signaling moiety, and play central roles in differentiation, homeostasis, and communications of all immunocyte lineages. As a resource to better understand their range and specificity of action, we profiled by RNAseq the immediate-early responses to the main γc cytokines across all immunocyte lineages. The results reveal an unprecedented landscape: broader, with extensive overlap between cytokines (one cytokine doing in one cell what another does elsewhere) and essentially no effects unique to any one cytokine. Responses include a major downregulation component and a broad Myc-controlled resetting of biosynthetic and metabolic pathways. Various mechanisms appear involved: fast transcriptional activation, chromatin remodeling, and mRNA destabilization. Other surprises were uncovered: IL2 effects in mast cells, shifts between follicular and marginal zone B cells, paradoxical and cell-specific cross-talk between interferon and γc signatures, or an NKT-like program induced by IL21 in CD8+ T cells.

Background/Context: Student loans reflect a larger shift in U.S. society in which people are forced to go into debt for basic needs. Student loan debt in the United States has been recognized as a political economic crisis that disproportionately devastates Black people. Scholars have statistically reported on racialized and gendered stratification in student loan outcomes and several name the racial wealth gap as the main contributing factor to the Black student debt crisis. Yet minimal attention has been dedicated to examining, let alone theorizing, the logics and systemic forces that racialize debt in higher education. Purpose: Drawing on a theory of racial capitalism, this article fills analytic and theoretical gaps in the study of the Black student debt crisis by detailing how the crisis has been arranged as well as how it functions to constrain, dispossess, and exploit Black people. Research Design: This article offers a corrective history, systematic analysis, and theoretical explanation of the Black student debt crisis. Findings/Results: The paper draws on racial capitalism to account for how student loans as a policy has relied on anti-Black racial logics and systemic forces. The authors address how Black educational desires are co-opted, the government configures inclusion according to predatory terms, and the student loan industry forms a debt trap that exploits repayment struggles. While the majority of Black people who enroll in higher education never secure the promise of college as always "worth it," the arrangement continues to be worthwhile for student loan profiteers. Student loans are perfect for racial capitalism because they answer demands for social access and inclusion (which are already reduced to mean credentialism) and reproduce both the disposability and dispossession of Black people's everyday lives. Conclusions/Recommendations: The authors call for the full cancellation of student loan debt. This call forms part of a larger mobilization to abolish the racist logics, processes, and policies that make the Black student debt crisis and Black precarity possible in the first place.

Numerous sectors and institutions engage in 'predatory inclusion', purporting to satisfy the unmet needs of historically marginalized groups under exploitative terms. However, extant scholarship has yet to robustly examine why they target certain groups. Drawing on Black feminist Marxism, I theorize how predatory inclusion depends on precarity, and I redefine 'precarity' as a structural position of vulnerability to violence based on excess responsibilities and the denial of means to meet them – or, 'alternativelessness'. I convey the usefulness of my definition of precarity and my theorization of the relationship between precarity and predatory inclusion through empirical sections that demonstrate how for-profit colleges ('for-profits') prey upon the alternativelessness of Black women, the race-gender demographic group with the highest rates of debt-financed enrollment in for-profits. By examining the training materials for admissions 'counselors' at for-profits, I illuminate how for-profits succeed at enrollment growth by manipulating the pain, urgency, and relationality of this precarity. I also reveal how descriptive statistics of Black women's enrollment and financial need in for-profits correspond to the sector's predation of precarity. I contend that precarity must be contested for the sake of ending the predatory inclusion of Black women and all others positioned alongside them as ideal prey. [ABSTRACT FROM AUTHOR]

In this review, we integrate three bodies of scholarship—education stratification research, political-historical sociology of higher education, and sociological theories of race and racism—to understand the production of "separate and unequal" postsecondary experiences for racially marginalized college students in the United States. We argue that the US postsecondary system is plural, heterogeneous, and stratified partly as a result of hundreds of years of contested efforts to deploy higher education in the service of white supremacy and capital accumulation. Organizational stratification of higher education along racial lines leads to horizontal stratification in individual experiences within the same level of schooling, and even within the same university. We review literature on racialized sorting between schools, which channels racially marginalized students to different parts of the postsecondary system relative to their racially advantaged peers. We also describe stratification within schools, as students are tracked, often by race, into divergent academic and social pathways internal to a single university. Both types of sorting have racial consequences for students' career trajectories, economic security, and well-being. Finally, we detail recent efforts to challenge horizontal stratification, responses to those efforts, and avenues for future research. [ABSTRACT FROM AUTHOR]

Breast cancer is characterized by histological and functional heterogeneity, posing a clinical challenge for patient treatment. Emerging evidence suggests that the distinct subtypes reflect the repertoire of genetic alterations and the target cell. However, the precise initiating events that predispose normal epithelium to neoplasia are poorly understood. Here, we demonstrate that breast epithelial organoids can be generated from human reduction mammoplasties (12 out of 12 donors), thus creating a tool to study the clonal evolution of breast cancer. To recapitulate de novo oncogenesis, we exploited clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 for targeted knockout of four breast cancer-associated tumor suppressor genes (P53, PTEN, RB1, NF1) in mammary progenitor cells from six donors. Mutant organoids gained long-term culturing capacity and formed estrogen-receptor positive luminal tumors on transplantation into mice for one out of six P53/PTEN/RB1-mutated and three out of six P53/PTEN/RB1/NF1-mutated lines. These organoids responded to endocrine therapy or chemotherapy, supporting the potential utility of this model to enhance our understanding of the molecular events that culminate in specific subtypes of breast cancer. [ABSTRACT FROM AUTHOR]

Breast cancer is characterized by histological and functional heterogeneity, posing a clinical challenge for patient treatment. Emerging evidence suggests that the distinct subtypes reflect the repertoire of genetic alterations and the target cell. However, the precise initiating events that predispose normal epithelium to neoplasia are poorly understood. Here, we demonstrate that breast epithelial organoids can be generated from human reduction mammoplasties (12 out of 12 donors), thus creating a tool to study the clonal evolution of breast cancer. To recapitulate de novo oncogenesis, we exploited clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 for targeted knockout of four breast cancer-associated tumor suppressor genes (P53, PTEN, RB1, NF1) in mammary progenitor cells from six donors. Mutant organoids gained long-term culturing capacity and formed estrogen-receptor positive luminal tumors on transplantation into mice for one out of six P53/PTEN/RB1-mutated and three out of six P53/PTEN/RB1/NF1-mutated lines. These organoids responded to endocrine therapy or chemotherapy, supporting the potential utility of this model to enhance our understanding of the molecular events that culminate in specific subtypes of breast cancer., (© The Author(s) 2019. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.)